Particulate air pollution has been associated with cardiovascular deaths and morbidity, but the mechanisms behind those associations are not folly understood. Having diabetes or pre-existing coronary artery disease increases the particle-associated risk for cardiac morbidity. Diabetics may be at increased risk because air pollution disturbs the same pathways as diabetes ? inflammation, vascular/endothelial and autonomic function. In a repeated measures Boston prospective study including 45 non-smoking subjects with Type 2 diabetes and 45 subjects with coronary artery disease observed every other week for 5 total visits (450 repeated measures) we hypothesize that:(l) Vascular and endothelial function (e.g., basal arterial diameter, endothelium-dependent vascular reactivity);pulmonary and systemic inflammation, and autonomic function (e.g, heart rate variability) are adversely affected by particulate air pollution;and (2) Vascular and endothelial function (e.g., basal arterial diameter, endothelium-dependent vascular reactivity), inflammatory markers, and autonomic function will vary with level of (a) traffic-related particles levels, as indexed by black carbon, and (b) long-range transport particles levels, as indexed by SO4. Pollution exposure will be estimated through central site (e.g, continuous PM2.5, black carbon;24-h integrated SO4), personal (i.e., continuous PM2.5;24-h integrated PMa.s, black carbon (particle reflectance), and SO4), and community level measures. Outcome measures will include brachial artery diameter, endothelium-dependent flow mediated dilation, augmentation index, exhaled NO (marker of pulmonary inflammation), markers of systemic inflammation/endothelial activation (WBC, fibrinogen, C-reactive protein, IL-6, TNF-a;sICAM-1, sVCAM-1, endothelin-1), and heart rate variability. This study will provide additional insight into the mechanisms whereby ambient pollution is associated with excess cardiac risk and may provide clues as to how to develop preventive strategies to reduce this risk.